A small molecule enhances arrestin-3 binding to the β-adrenergic receptor.

G protein-coupled receptor (GPCR) signaling is terminated by arrestin binding to a phosphorylated receptor. Binding propensity has been shown to be modulated by stabilizing the pre-activated state of arrestin through point mutations or C-tail truncation. Here, we hypothesize that pre-activated rotated states can be stabilized by small molecules, and this can promote binding to phosphorylation-deficient receptors, which underly a variety of human disorders.

A new era in neuromuscular junction research: current advances in self-organized and assembled in vitro models.

Understanding the development and function of the human neuromuscular system is crucial for deciphering the mechanisms of neuromuscular disorders and developing effective therapies. However, limitations of animal models necessitate the development of human-specific in vitro models to study such complex diseases effectively. Here, we discuss different approaches for in vitro neuromuscular junction (NMJ) modeling: complex self-organized models that rely on the inherent abilities of cells to form NMJs based on embryonic developmental principles and assembled models that depend on integrating different cell types for controlled NMJ formation.

High-resolution mapping of sensory fibers at the healthy and post-myocardial infarct whole transgenic hearts.

The sensory nervous system is critical to maintain cardiac function. As opposed to efferent innervation, less is known about cardiac afferents. For this, we mapped the VGLUT2-expressing cardiac afferent fibers of spinal and vagal origin by using the VGLUT2::tdTomato double transgenic mouse as an approach to visualize the whole hearts both at the dorsal and ventral sides.

Anatomical characterization of vagal nodose afferent innervation and ending morphologies at the murine heart using a transgenic approach.

Heart is an extensively innervated organ and its function is strictly coordinated by autonomic neural circuits. After pathological events such as myocardial infarction (MI), cardiac nerves undergo a structural and functional remodeling contributing to cardiac dysfunction. Although the efferent component of the cardiac nerves has been well described, sensory innervation of the heart has not been defined in detail.